ArticleThe Biochemical journal2007
Induced JunD in intestinal epithelial cells represses CDK4 transcription through its proximal promoter region following polyamine depletion.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
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- Gastrointestinal toxicity associated with cyclin-dependent kinase 4/6 inhibitors in breast cancer patients: insights from a real-world pharmacovigilance analysis.Frontiers in medicine · 2026Article
- Role of polyamines in intestinal mucosal barrier function.Seminars in immunopathology · 2025Review
- CHREBP suppresses gastric cancer progression via the cyclin D1-Rb-E2F1 pathway.Cell death discovery · 2022Article
- Polyamines: Functions, Metabolism, and Role in Human Disease Management.Medical sciences (Basel, Switzerland) · 2021Review
- lncRNA RP11-624L4.1 Is Associated with Unfavorable Prognosis and Promotes Proliferation via the CDK4/6-Cyclin D1-Rb-E2F1 Pathway in NPC.Molecular therapy. Nucleic acids · 2020Article
- Polyamine Metabolism and Oxidative Protein Folding in the ER as ROS-Producing Systems Neglected in Virology.International journal of molecular sciences · 2018Review
- c-Jun enhances intestinal epithelial restitution after wounding by increasing phospholipase C-γ1 transcription.American journal of physiology. Cell physiology · 2017Article
- Transcriptional regulation of importin-α1 by JunD modulates subcellular localization of RNA-binding protein HuR in intestinal epithelial cells.American journal of physiology. Cell physiology · 2016Article
- JunD enhances miR-29b levels transcriptionally and posttranscriptionally to inhibit proliferation of intestinal epithelial cells.American journal of physiology. Cell physiology · 2015Article
- RNA-binding proteins and microRNAs in gastrointestinal epithelial homeostasis and diseases.Current opinion in pharmacology · 2014Review
- Combined ChIP-Seq and transcriptome analysis identifies AP-1/JunD as a primary regulator of oxidative stress and IL-1β synthesis in macrophages.BMC genomics · 2013Article
- Depletion of the p43 mitochondrial T3 receptor increases Sertoli cell proliferation in mice.PloS one · 2013Article
- Competitive binding of CUGBP1 and HuR to occludin mRNA controls its translation and modulates epithelial barrier function.Molecular biology of the cell · 2013Article
- Polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca²+ signaling by differentially modulating STIM1 and STIM2.American journal of physiology. Cell physiology · 2012Article
- Polyamines and Gut Mucosal Homeostasis.Journal of gastrointestinal & digestive system · 2012Article
- JunD/AP-1-mediated gene expression promotes lymphocyte growth dependent on interleukin-7 signal transduction.PloS one · 2012Article
- Regulation of cyclin-dependent kinase 4 translation through CUG-binding protein 1 and microRNA-222 by polyamines.Molecular biology of the cell · 2011Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Maintenance of intestinal epithelial integrity requires cellular polyamines that regulate expression of various genes involved in cell proliferation, growth arrest and apoptosis. In prior studies, depletion of cellular polyamines has been shown to stabilize JunD, a member of the AP-1 (activator protein-1) family of transcription factors, leading to inhibition of intestinal epithelial cell proliferation, but the exact downstream targets of induced JunD remain elusive. CDK4 (cyclin-dependent kinase 4) is essential for the G1- to S-phase transition during the cell cycle and its expression is primarily controlled at the transcriptional level. In the present study, we show that induced JunD in IECs (intestinal epithelial cells) is a transcriptional repressor of the CDK4 gene following polyamine depletion. Increased JunD in polyamine-deficient cells was associated with a significant inhibition of CDK4 transcription, as indicated by repression of CDK4-promoter activity and decreased levels of CDK4 mRNA and protein, all of which were prevented by using specific antisense JunD oligomers. Ectopic expression of the wild-type junD also repressed CDK4-promoter activity and decreased levels of CDK4 mRNA and protein without any effect on CDK2 expression. Gel shift and chromatin immunoprecipitation assays revealed that JunD bound to the proximal region of the CDK4-promoter in vitro as well as in vivo, while experiments using different CDK4-promoter mutants showed that transcriptional repression of CDK4 by JunD was mediated through an AP-1 binding site within this proximal sequence of the CDK4-promoter. These results indicate that induced JunD in IECs represses CDK4 transcription through its proximal promoter region following polyamine depletion.
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